Exercise recovery increases skeletal muscle HO emission and mitochondrial respiratory capacity following two-weeks of limb immobilization.

Extended periods of skeletal muscle disuse result in muscle atrophy. Following limb immobilization, increased mitochondrial reactive oxygen species (ROS) production may contribute to atrophy through increases in skeletal muscle protein degradation. However, the effect of skeletal muscle disuse on mitochondrial ROS production remains unclear. This study investigated the effect of immobilization, followed by two subsequent periods of restored physical activity, on mitochondrial HO emissions in adult male skeletal muscle. Middle-aged men (n = 30, 49.7 ± 3.84 y) completed two weeks of unilateral lower-limb immobilization, followed by two weeks of baseline-matched activity, consisting of 10,000 steps a day, then completed two weeks of three times weekly supervised resistance training. Vastus lateralis biopsies were taken at baseline, post-immobilization, post-ambulatory recovery, and post-resistance-training. High-resolution respirometry was used simultaneously with fluorometry to determine mitochondrial respiration and hydrogen peroxide (HO) production in permeabilized muscle fibres. Mitochondrial HO emission with complex I and II substrates, in the absence of ADP, was greater following immobilization, however, there was no effect on mitochondrial respiration. Both ambulatory recovery and resistance training, following the period of immobilization, increased in mitochondrial HO emissions. These data demonstrated that 2 weeks of immobilization increases mitochondrial HO emissions, but subsequent retraining periods of ambulatory recovery and resistance training also led to in robust increases in mitochondrial HO emissions in skeletal muscle.